Functional Role of Female Sex Hormones and Receptors in Cervical Carcinoma

Cervical carcinoma remains one of the most prevalent malignancies affecting women worldwide. While human papillomavirus (HPV) infection is a well-established etiological factor, growing evidence suggests that female sex hormones and their receptors may significantly influence the pathogenesis and progression of cervical cancer. Hormonal imbalances, particularly involving estrogen and progesterone, may impact tumor growth and immune modulation within the tumor microenvironment. This study investigates the functional role of selected female sex hormones and their corresponding receptors in Iraqi women diagnosed with cervical carcinoma. A total of 60 female participants were enrolled from gynecology and oncology departments in Baghdad and Karbala, Iraq. Thirty women with histologically confirmed cervical carcinoma were assigned to the patient group, while thirty age-matched healthy volunteers served as controls. Blood samples were collected under fasting conditions, and serum levels of sex hormone-binding globulin (SHBG), estradiol (E2), dehydroepiandrosterone sulfate (DHEAS), progesterone, estrogen receptor alpha (ERα), and progesterone receptor (PR) were quantified using standardized ELISA kits. Statistical comparisons were conducted using SPSS with significance set at p < 0.05. Significant hormonal differences were observed between patient and control groups. Estradiol levels were markedly lower in postmenopausal patients than in premenopausal patients, while DHEAS levels were significantly higher in the same comparison. SHBG and DHEAS levels were also elevated in patients compared to controls. Importantly, ERα levels were significantly decreased, while PR levels were significantly increased in cervical cancer patients relative to controls. A strong association was observed between cervical cancer diagnosis and positive family history (73.3% in patients vs. 13% in controls). Our findings suggest that imbalances in circulating sex hormones and alterations in receptor expression—particularly reduced ERα and elevated PR, may contribute to cervical carcinogenesis. These hormonal and biochemical signatures, alongside potential hereditary patterns, highlight the importance of incorporating hormonal profiling in the clinical evaluation of cervical cancer. Further research is warranted to explore the therapeutic potential of targeting hormone receptor pathways in cervical cancer management.